The effects of allitridin on the expression of transcription factors T-bet and GATA-3 in mice infected by murine cytomegalovirus.
J Med Food. 2005;8(3):332-6. PMID: 16176143
This study was designed to investigate the effects of allitridin on the expression of transcription factors T-bet and GATA-3 in mice infected by murine cytomegalovirus (MCMV). A BALB/c mouse model system of MCMV infection was established. Twenty mice were allocated randomly into an allitridin-treated group (n = 10) and a placebo control group (n = 10). The same dose (25 mg/kg/day) and regimen of allitridin were used in the treated group in the 24 hours after virus infection; the same volume of saline solution was injected in placebo control mice. In an additional blank control group (n = 10), the same volume of saline solution was injected. The expression levels of the transcription factors T-bet and GATA-3 were measured by reverse transcription-polymerase chain reaction. The expression levels of the T helper (Th) 1 cytokine interferon-gamma (IFN-gamma) and the Th2 cytokine interleukin (IL)-10 in supernatant of spleen cell culture were measured by enzyme-linked immunosorbent assay. MCMV infection markedly down-modulated the expression of IFN-gamma and T-bet and significantly up-modulated the expression of IL-10 and GATA-3. Allitridin induced significantly (P<.01) increased expression of the transcription factor T-bet and the Th1 cytokine IFN-gamma and markedly (P<.01) decreased expression of the transcription factor GATA-3 and the Th2 cytokine IL-10. Thus MCMV infection could lead to disequilibrium of Th1/Th2 cytokine expression: The level of the Th1 cytokine IFN-gamma was decreased significantly, and Th2 cytokine IL-10 was overexpressed markedly. Allitridin could up-regulate the expression of T-bet and IFN-gamma and inhibit the expression of GATA-3 and IL-10 in MCMV-infected mice, indicating a Th1 dominant state, which should enhance the specific cellular immune reactions against cytomegalovirus (CMV) and be helpful for clearance of CMV from the host.